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Objective To investigate the impact of tanshinone Ⅱ A on the level of brain NMDAR1 protein in rats after cardiopulmonary resuscitation and its effects of brain function protection.Methods Seventy-eight SD male rats were randomly (random number) divided into three groups:group A (sham group,n =6),group B (control group,n =36) and group C (Tanshinone Ⅱ A intervention group,n =36).All animals were induced to be models of cardiac arrest by choking.The rats of group C received intravenous injection of Tanshinone Ⅱ A in dose of 15 mg/kg immediately at initiation of resuscitation,while rats of group B were intravenous injected same amount of normal saline instead.Brains tissues of all rats were taken at 1,6,12,24,48 and 72 h after the restoration of spontaneous circulation (ROSC).Immunohistochemical staining method was applied for measuring the levels of brain tissue NMDAR1 and Caspases-3,while water content of the brain was detected by wet and dry weight ratio.The experimentaldata were analyzed by using one-way ANOVA.Results (①)The level of brain NMDAR1 protein in group B increased at 1 h and reached its peak at 6 h after ROSC,then its level gradually declined and dropped below normal at 48 h,72 h,and there were significant difference in variation of NMDAR1 protein levels in comparison with the group A (P ＜ 0.05) ; the NMDAR1 protein levels at 1,6,12 h in group C were significantly lower than those in group B at the same intervals (P ＜ 0.01),but no significant differences were seen at 24,48,72 h (P ＞ 0.05).(②)The level of brain Caspases-3 in group B increased after ROSC,and reached its peak at 48 h after ROSC,then declined and maintained above normal at 72 h,and this variation was significantly different from that of the group A (P ＜ 0.01) ; while the levels of caspase-3 at 1,6,12,24 h in group C were significantly lower than those in group B (P ＜ 0.01),but thses differences at 48,72 h were still significant (P ＜ 0.05).(③)The water content of brain tissue in group B increased at 1 h and reached its peak at 24 h after ROSC,then gradually decreased from 48 h,but maintained above normal at 72 h,and this trend of variation was significantly different from that of group A (P ＜ 0.01 or P ＜ 0.05).Compared with group B,water content of brain tissue in group C decreased more significantly (P ＜ 0.01).Conclusions Tanshinone Ⅱ A down-regulates brain NMDAR1 protein level at early stage in rats as well as significantly inhibits the level of Caspases-3 thereby ameliorating brain edema after cardiopulmonary resuscitation.
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Objective To investigate protective effects of the hydrogen saturated saline on acute lung injury and pulmonary fibrosis in rats with paraquat (PQ) poisoning. Method Forty-eight Sprague-Dawley rats were randomly divided into 3 groups, namely control group, PQ poisoning group and intervention group (n = 16 rats in each group) . Animals in PQ poisoning group and intervention group were fed with PQ in dosage of 50 mg / kg. Rats of control group were fed equivalent amount of distilled water instead. One hour after administration of PQ, rats of intervention group were treated with 5 ml / kg hydrogen saturated saline injected intra-peritoneally twice a day until the rats were sacrificed. The rats of poisoning group and control group were treated with intra-peritoneal injection of equivalent amount of normal saline. Arterial partial pressure of oxygen ( PaO2 ), 8-hydroxy-2' -desoxyguanosine (8-OHDG) and transforming growth factor β1 (TGF-β1) of lung tissue were measured on the 3rd and 21st day after PQ administration. Quantitative data was expressed as mean ±standard deviation (x-±s) . SPSS version 12. 0 package was applied for variance analysis and SNK-q test, and statistical differences were considered significant when P ＜ 0. 05. Results ① PaO2 decreased significantly in poisoning group (9. 34 ± 0. 47 kPa) and intervention group (10. 30±0.62 kPa) compared with control group (11.87 +/- 0.42 kPa) on the 3d (P ＜0.01), and as intervention group was compared with poisoning group, there was a significant difference ( P ＜ 0. 05 ) . On the 21st day, PaO2 was still lower in poisoning group (8. 36 ±0. 51 kPa) and intervention group ( 10. 14 ±0. 27 kPa) than that in control group ( 11.87 +0. 24 kPa) (P ＜0. 01 and P ＜0. 05, respectively), and as intervention group was compared with poisoning group, there was a significant difference ( P ＜ 0. 01 ) . ②The levels of 8-OHDG in lung tissue increased significantly in poisoning group (23.58±7. 18 ng/ml ) and intervention group (9. 49± 2. 45 ng/ml) on the 3rd day after PQ administration compared with control group (7.71 + 1.96 ng/ml) (P＜0. 01 and P＜0. 05, respectively), and as intervention group was compared with poisoning group there was a significant difference ( p ＜0. 01 ) . There were no significant differences in 8-OHDG level found among the groups on the 21st day after PQ administration (P ＞ 0. 05 ) . ③ The level of TGF-β1 (measured by mean optic density, MOD) in lung tissue of rats in poisoning group ( 10. 11±2.49 MOD) and intervention group (8. 14 + 1.58 MOD) exhibited in higher levels than control group (5.93 + 1. 98 MOD) on the 3rd and (5.97 + 2. 35 MOD) on the 21st day after PQ administration (P ＜0. 01 and P ＜0. 05, respectively), and however, a lower level of TGF-β1 was observed in intervention group on 3d and 21d compared with poisoning group (P ＜0. 05 and P ＜0. 01, respectively) . Conclusions Hydrogen saturated saline can alleviate oxidative stress, mitigate oxidative damage and inhibit pulmonary fibrosis of lung induced by PQ intoxication.
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ObjectiveTo investigate the nutritional risk incidence and clinical outcome in.hospitalized patients with liver diseases.MethodsThe data of 390 cases of liver disease inpatients were studied.The nutritional status of the enrolled patients was assessed with Nutritional Risk Screening 2002.ResultsThe total incidence of nutritional risk in the liver disease patients was 47.95％.The incidence was 81.82％ in severe hepatitis patients,significantly higher that that in acute hepatitis patients (43.33％,P =0.013) and chronic hepatitis patients (28.30％,P =0.000).The incidence of nutritional risk was 75.79％ in hepatic cirrhosis patients,also significantly higher than that in acute hepatitis patients (P =0.000) and chronic hepatitis patients (P =0.000).ConclusionSevere hepatitis and hepatic cirrhosis patients may have higher nutritional risk than acute and chronic hepatitis patients.